Anti-inflammatory potential of β-cryptoxanthin against LPS-induced inflammation in mouse Sertoli cells

• CX inhibits the LPS-induced cell apoptosis.
• CX also inhibits LPS-induced down-regulation of spermatogenesis related genes.
• CX inhibits LPS-induced up-regulation of TNF-α, IL10, IL-6 and IL-1β through NF-κB activation and MAPK of phosphorylation.

β-cryptoxanthin (CX), a major carotenoid pigment, can inhibit inflammatory gene expression in mice with nonalcoholic steatohepatitis. In the present study, we examined the anti-inflammatory effects of CX on lipopolysaccharide (LPS)-induced inflammation in mouse primary Sertoli cells and the possible molecular mechanisms behind its effects. The results showed that CX significantly inhibited LPS-induced decreases in cell viability and in the percentage of apoptotic cells. Moreover, CX inhibited the LPS-induced up-regulation of tumor necrosis factor α (TNF-α), interleukin-10 (IL-10), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in Sertoli cells. In addition, CX significantly limited the LPS-induced down-regulation of AR, HSF2, CREB, FSHR, INHBB and ABP in Sertoli cells. Western blot analysis showed that CX significantly suppressed NF-κB (p65) activation as well as MAPK phosphorylation. All the results suggested that CX suppressed inflammation, possibly associated with the NF-κB activation and MAPK of phosphorylation. Thus, CX may possess therapeutic potential against inflammation-related diseases.

Sertoli cells were stimulated with LPS for 24 h, and then treated with CX (15 μM) for 48 h. The results showed that CX significantly inhibited LPS-induced decreases in cell viability and in the percentage of apoptotic cells.Figure optionsDownload as PowerPoint slide